The present invention relates to a method for regulating potency of pluripotent stem cells (PSCs) by modulating expression of podocalyxin-like protein 1 (PODXL) and applications thereof.

The present invention relates to a method for regulating potency of pluripotent stem cells (PSCs) by modulating expression of podocalyxin-like protein 1 (PODXL) and applications thereof.

The present invention features compositions and methods for recapitulating physiological X-chromosome inactivation (XCI) in a cell, including a cell of any embryo generated by Somatic Cell Nuclear Transfer (SCNT). In one aspect, the invention features a method for generating physiological X chromosome inactivation in an embryo generated by SCNT, the method comprising injecting the embryo generated via SCNT with an H3K27me3-specific demethylase polypeptide or a polynucleotide encoding said demethylase. Disclosed herein are methods, compositions, and kits comprising an agent which increases the expression of genes encoding an H3K27me3-specific demethylase, or increases the activity of human H3K27me3-specific demethylase.

A device and a method are disclosed for collecting and culturing fish embryos and evaluating combined toxicity of thiamethoxam and tetraconazole. An embryo collection component and an embryo culture component are provided on a base plate. The embryo collection component includes a collection tray detachably connected to a bottom of a culture tube. The embryo culture component includes a cavity plate with a stopper inside and a top plate provided with a culture well. A bottom of the culture well is provided with a leakage hole; and after the top plate is installed into the cavity plate, the stopper occludes the leakage hole. The new device is used to carry out the combined toxicity effect test of thiamethoxam and tetraconazole on zebrafish embryos, which can be used to avoid development of pesticide mixtures that have a good preventive effect but pose increased toxicity risk to the ecological environment.

The present invention provides ungulate animals, tissue and organs as well as cells and cell lines derived from such animals, tissue and organs, which lack expression of functional endogenous immunoglobulin loci. The present invention also provides ungulate animals, tissue and organs as well as cells and cell lines derived from such animals, tissue and organs, which express xenogenous, such as human, immunoglobulin loci. The present invention further provides ungulate, such as porcine genomic DNA sequence of porcine heavy and light chain immunogobulins. Such animals, tissues, organs and cells can be used in research and medical therapy. In addition, methods are provided to prepare such animals, organs, tissues, and cells.

The present invention provides ungulate animals, tissue and organs as well as cells and cell lines derived from such animals, tissue and organs, which lack expression of functional endogenous immunoglobulin loci. The present invention also provides ungulate animals, tissue and organs as well as cells and cell lines derived from such animals, tissue and organs, which express xenogenous, such as human, immunoglobulin loci. The present invention further provides ungulate, such as porcine genomic DNA sequence of porcine heavy and light chain immunogobulins. Such animals, tissues, organs and cells can be used in research and medical therapy. In addition, methods are provided to prepare such animals, organs, tissues, and cells.

Fish embryos may be successfully vaccinated or therapeutically treated if the therapeutic agent is injected into the yolk sac. Therapeutic agents may be directly injected or released from microspheres and enter the circulation and tissues. Injection into the yolk sac, combined with the use of carriers, allows for a continued, controlled release of therapeutic agents and processing of antigens. Fish vaccination or therapeutic treatment, selecting fish embryos post fertilization at the one-cell to eyed egg stage of development, and injecting the yolk sac with carriers associated with an antigen(s) or therapeutic agent(s), may be fully automated.

Fish embryos may be successfully vaccinated or therapeutically treated if the therapeutic agent is injected into the yolk sac. Therapeutic agents may be directly injected or released from microspheres and enter the circulation and tissues. Injection into the yolk sac, combined with the use of carriers, allows for a continued, controlled release of therapeutic agents and processing of antigens. Fish vaccination or therapeutic treatment, selecting fish embryos post fertilization at the one-cell to eyed egg stage of development, and injecting the yolk sac with carriers associated with an antigen(s) or therapeutic agent(s), may be fully automated.

The present disclosure provides methods to produce non-human animal models for diseases that have a poor life-expectancy. The animal models provided herein are the result of gene editing to result in genetic lesions that recapitulate human diseases by virtue of introgressing lethal, dominant negative or non-functional mutations in animal genomes corresponding to those responsible for human diseases. In some cases, the genomic edit may result in a low number of pregnancies carried to term and/or a failure to thrive phenotype with those born failing to survive to sexual maturity. The present disclosure provides methods to produce non-chimeric animals containing a detrimental genetic lesion from healthy chimeric animals. In this method, the chimeric animals are derived from cells in which the genetic lesion is made with the defect being complemented by the genome of an animal that is gametogenically deficient (cannot produce gametes) and cannot pass on its own genes. Thus, the gametes of the chimera are completely derived from the edited animal. When a male and female chimera are mated with each other, the offspring are 100% of the edited genome.

The present disclosure provides methods to produce non-human animal models for diseases that have a poor life-expectancy. The animal models provided herein are the result of gene editing to result in genetic lesions that recapitulate human diseases by virtue of introgressing lethal, dominant negative or non-functional mutations in animal genomes corresponding to those responsible for human diseases. In some cases, the genomic edit may result in a low number of pregnancies carried to term and/or a failure to thrive phenotype with those born failing to survive to sexual maturity. The present disclosure provides methods to produce non-chimeric animals containing a detrimental genetic lesion from healthy chimeric animals. In this method, the chimeric animals are derived from cells in which the genetic lesion is made with the defect being complemented by the genome of an animal that is gametogenically deficient (cannot produce gametes) and cannot pass on its own genes. Thus, the gametes of the chimera are completely derived from the edited animal. When a male and female chimera are mated with each other, the offspring are 100% of the edited genome.